Claude A. Piantadosi, MD; David A. Schwartz, MD, MPH
Grant Support: By the National Heart, Lung, and Blood Institute, National Institutes of Health (PO1 HL 31992-18).
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Claude A. Piantadosi, MD, Division of Pulmonary and Critical Care Medicine, Box 3315, Duke University Medical Center, Durham, NC 27710; e-mail, firstname.lastname@example.org.
Current Author Addresses: Dr. Piantadosi: Division of Pulmonary and Critical Care Medicine, Box 3315, Duke University Medical Center, Durham, NC 27710.
Dr. Schwartz: Division of Pulmonary and Critical Care Medicine, Box 2629, Duke University Medical Center, Durham, NC 27710.
Piantadosi C., Schwartz D.; The Acute Respiratory Distress Syndrome. Ann Intern Med. 2004;141:460-470. doi: 10.7326/0003-4819-141-6-200409210-00012
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Published: Ann Intern Med. 2004;141(6):460-470.
Severe respiratory distress and 1 or more risk factors (including infection, aspiration, pancreatitis, and trauma)
Impaired arterial oxygenation (hypoxemia)
Bilateral pulmonary infiltrates on chest radiograph
No clinical evidence of elevated left atrial pressure (or pulmonary artery occlusion pressure of ≤ 18 mm Hg if measurements are available)
The cardinal feature of ARDS, refractory hypoxemia, is caused by formation of protein-rich alveolar edema after damage to the integrity of the lung's alveolar-capillary barrier.
Alveolar-capillary damage in ARDS can be initiated by physical or chemical injury or by extensive activation of innate inflammatory responses. Such damage causes the lung's edema safety factor to decrease by about half, and edema develops at low capillary pressures.
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Pulmonary/Critical Care, Acute Respiratory Distress Syndrome/Acute Lung Injury.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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